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April 16, 2026ACS Omega0 citationsOpen Access

ROS-Responsive Hydrogel Loaded with Antimicrobial Peptides Accelerated Infected Wound Healing

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ZNZefan NiuYLYunzhe LiQYQing Yuan

Key Points

  • The aim is to develop a hydrogel that responds to reactive oxygen species to improve infected wound healing.
  • Synthesis of ROS-responsive hydrogel using hyaluronic acid and phenylboronic acid.
  • Cross-linking the hydrogel with PVA in a ROS-sensitive bond.
  • Loading the hydrogel with antimicrobial peptides for enhanced effects.
  • Conducting in vitro assessments for biocompatibility and antibacterial properties.
  • Performing in vivo experiments on infected mice to evaluate healing effectiveness.
  • The hydrogel showed significant inhibition of E. coli and S. aureus growth.
  • In vivo results indicated accelerated healing of infected wounds in mice.
  • The hydrogel increased IL-6 and TGF-β levels at the wound site.
  • Reduction in inflammation at the wound was observed after treatment.
  • Enhanced expression of CD31 and VEGF levels indicated improved angiogenesis.

Abstract

Skin injury triggers the production of reactive oxygen species (ROS) such as H2O2 in the wound microenvironment. In addition to ROS produced by the wound itself, ROS produced by bacterial infections likewise cause severe damage to blood vessels and endothelial cells, leading to chronic or unhealed wounds. Hyaluronic acid (HA) is widely used in hydrogel construction due to its rich bioactivity. In this study, an antibacterial hydrogel with ROS responsiveness was synthesized by grafting HA through phenylboronic acid, cross-linking it with PVA in a ROS-sensitive phenylboron ester bond, and loading it with AMP for the treatment of bacterial-infected wounds. In vitro experiments proved that the hydrogel has good biocompatibility, antioxidant ability, and significant inhibition of E. coli and S. aureus. In vivo experiments proved that the hydrogel promotes the healing of infected wounds in mice, raises the level of IL-6/TGF-β at the wounds, reduces the inflammation of the wounds, raises the level of expression of CD31/VEGF, and promotes the angiogenesis of wounds.

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Cite This Study

Niu et al. (2026) studied this question.

synapsesocial.com/papers/69e07c632f7e8953b7cbd9b2https://doi.org/10.1021/acsomega.5c06194
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